Neural function during emotion processing and modulation associated with treatment response in a randomized clinical trial for posttraumatic stress disorder.
Cognitive Behavioral Therapy
PTSD
functional MRI
pharmacotherapy
trauma
Journal
Depression and anxiety
ISSN: 1520-6394
Titre abrégé: Depress Anxiety
Pays: United States
ID NLM: 9708816
Informations de publication
Date de publication:
07 2020
07 2020
Historique:
received:
11
07
2019
revised:
19
02
2020
accepted:
27
03
2020
pubmed:
20
4
2020
medline:
21
11
2020
entrez:
20
4
2020
Statut:
ppublish
Résumé
Posttraumatic stress disorder (PTSD) has been associated with exaggerated threat processing and deficits in emotion modulation circuitry. It remains unknown how neural circuits are associated with response to evidence-based treatments for PTSD. We examined associations between PTSD symptoms and indicators of neural response in key emotion processing and modulation regions. Fifty-six military Veterans with PTSD were randomly assigned to one of three evidence-based treatments (prolonged exposure, sertraline, and PE plus sertraline) in a randomized clinical trial ("PROGrESS"; 2018, Contemp Clin Trials, 64, 128-138). Twenty-seven combat-exposed controls (CCs) served as a comparison group at pretreatment. Before and after PTSD treatment, functional magnetic resonance imaging was used to assess brain activation and connectivity during the validated Shifted Attention Emotion Appraisal Task (2003, J Neurosci, 23, 5627-5633; 2013, Biol Psychiatry, 73, 1045-1053). Greater activation in emotion processing (anterior insula) and modulation (prefrontal cortex) regions and increased connectivity between attentional control (dorsolateral prefrontal cortex and superior parietal cortex) and emotion processing (amygdala) regions, at pretreatment, were associated with subsequent PTSD symptom improvement. This study is one of the first to examine task-based activation and functional connectivity in a PTSD treatment trial, and provides evidence to suggest that activation in and connectivity between emotion processing and modulation regions are important predictors of treatment response.
Sections du résumé
BACKGROUND
Posttraumatic stress disorder (PTSD) has been associated with exaggerated threat processing and deficits in emotion modulation circuitry. It remains unknown how neural circuits are associated with response to evidence-based treatments for PTSD.
METHOD
We examined associations between PTSD symptoms and indicators of neural response in key emotion processing and modulation regions. Fifty-six military Veterans with PTSD were randomly assigned to one of three evidence-based treatments (prolonged exposure, sertraline, and PE plus sertraline) in a randomized clinical trial ("PROGrESS"; 2018, Contemp Clin Trials, 64, 128-138). Twenty-seven combat-exposed controls (CCs) served as a comparison group at pretreatment. Before and after PTSD treatment, functional magnetic resonance imaging was used to assess brain activation and connectivity during the validated Shifted Attention Emotion Appraisal Task (2003, J Neurosci, 23, 5627-5633; 2013, Biol Psychiatry, 73, 1045-1053).
RESULTS
Greater activation in emotion processing (anterior insula) and modulation (prefrontal cortex) regions and increased connectivity between attentional control (dorsolateral prefrontal cortex and superior parietal cortex) and emotion processing (amygdala) regions, at pretreatment, were associated with subsequent PTSD symptom improvement.
CONCLUSIONS
This study is one of the first to examine task-based activation and functional connectivity in a PTSD treatment trial, and provides evidence to suggest that activation in and connectivity between emotion processing and modulation regions are important predictors of treatment response.
Identifiants
pubmed: 32306485
doi: 10.1002/da.23022
pmc: PMC8010611
mid: NIHMS1681863
doi:
Banques de données
ClinicalTrials.gov
['NCT01524133']
Types de publication
Journal Article
Randomized Controlled Trial
Research Support, N.I.H., Extramural
Research Support, U.S. Gov't, Non-P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Pagination
670-681Subventions
Organisme : NIMH NIH HHS
ID : K23 MH109762
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR000433
Pays : United States
Organisme : US Department of Defense Medical Research and Materiel Command
ID : W81XWH-11-1-0073
Pays : International
Informations de copyright
© 2020 Wiley Periodicals, Inc.
Références
Psychother Psychosom. 2013;82(6):382-9
pubmed: 24061484
J Abnorm Psychol. 2010 Feb;119(1):241-7
pubmed: 20141261
Biol Psychiatry. 2010 Sep 1;68(5):433-41
pubmed: 20573339
Depress Anxiety. 2015 Dec;32(12):927-34
pubmed: 26522237
Cochrane Database Syst Rev. 2006 Jan 25;(1):CD002795
pubmed: 16437445
J Anxiety Disord. 2018 May;56:56-62
pubmed: 29729828
Biol Psychiatry. 2013 Jun 1;73(11):1045-53
pubmed: 23348009
Am J Psychiatry. 2017 Dec 1;174(12):1175-1184
pubmed: 28715907
JAMA Psychiatry. 2019 Feb 1;76(2):117-126
pubmed: 30516797
Biol Psychiatry. 2008 May 1;63(9):858-63
pubmed: 17964548
J Behav Ther Exp Psychiatry. 2014 Sep;45(3):360-7
pubmed: 24727342
Am J Psychiatry. 2007 Oct;164(10):1476-88
pubmed: 17898336
Ann N Y Acad Sci. 2010 Oct;1208:142-9
pubmed: 20955336
Am J Psychiatry. 2003 Mar;160(3):522-32
pubmed: 12611834
J Psychopharmacol. 2005 Nov;19(6):567-96
pubmed: 16272179
Contemp Clin Trials. 2018 Jan;64:128-138
pubmed: 29081351
Cogn Affect Behav Neurosci. 2017 Apr;17(2):422-436
pubmed: 27966102
Acta Psychiatr Scand Suppl. 2000;403:39-49
pubmed: 11019934
Arch Gen Psychiatry. 2006 Feb;63(2):184-92
pubmed: 16461862
J Clin Psychiatry. 1998;59 Suppl 20:22-33;quiz 34-57
pubmed: 9881538
CNS Spectr. 2003 Sep;8(9):641-50
pubmed: 15079138
Arch Gen Psychiatry. 2012 Apr;69(4):360-71
pubmed: 22474105
J Neurosci Res. 2016 Jun;94(6):535-43
pubmed: 26469872
Soc Cogn Affect Neurosci. 2015 Nov;10(11):1596-606
pubmed: 25939653
Depress Anxiety. 2012 May;29(5):449-59
pubmed: 22553009
PLoS One. 2016 Jul 14;11(7):e0159065
pubmed: 27415431
Curr Psychiatry Rep. 2013 May;15(5):358
pubmed: 23619614
Biol Psychiatry. 2000 May 1;47(9):769-76
pubmed: 10812035
J Neurosci. 2003 Jul 2;23(13):5627-33
pubmed: 12843265
Psychother Psychosom. 2013;82(3):142-51
pubmed: 23548778
Biol Mood Anxiety Disord. 2012 May 18;2:9
pubmed: 22738125
Neuroimage. 2014 Apr 1;89:110-21
pubmed: 24246489
J Psychiatr Res. 2013 Oct;47(10):1469-78
pubmed: 23827769
Biol Psychiatry. 2006 Aug 15;60(4):376-82
pubmed: 16919525
Psychol Med. 2013 Jan;43(1):85-95
pubmed: 22571775
Dialogues Clin Neurosci. 2006;8(4):445-61
pubmed: 17290802
Curr Top Behav Neurosci. 2012;11:289-320
pubmed: 22081443
J Rehabil Res Dev. 2012;49(5):679-87
pubmed: 23015579
Hum Brain Mapp. 2008 May;29(5):517-23
pubmed: 17525984
Psychol Bull. 2007 Sep;133(5):725-46
pubmed: 17723027
CNS Neurosci Ther. 2011 Aug;17(4):227-36
pubmed: 20406268
Cogn Behav Ther. 2018 Sep;47(5):351-371
pubmed: 29448886
Psychiatry Res Neuroimaging. 2020 May 30;299:111062
pubmed: 32278278
Depress Anxiety. 2011 Mar;28(3):194-201
pubmed: 21394852
Am J Psychiatry. 2017 Dec 1;174(12):1163-1174
pubmed: 28715908
J Trauma Stress. 1995 Jan;8(1):75-90
pubmed: 7712061